Musculoskeletal Flashcards
Basics of Bones and Joints
Arthritis
The hallmark of arthritis is cartilage destruction, which may be evident on radiographs as cartilage space narrowing.
In broad categories, arthritis can be divided into degenerative (osteoarthritis), inflammatory (rheumatoid arthritis, spondyloarthropathies, and juvenile idiopathic arthritis), crystal deposition (gout, calcium pyrophosphate dihydrate, and hydroxyapatite), hematologic (hemophilia), and metabolic changes.
Osteoarthitis overview
Also called osteoarthosis or degenerative joint disease, osteoarthritis (OA) is the result of articular cartilage breakdown from altered local mechanical factors in a susceptible individual. In addition to cartilage, OA is thought to involve the entire joint including bone, ligaments, menisci, joint capsule, synovium, and musculature.
OA is the most common cause of cartilage loss in the middle-aged and older population.
OA typically occurs in weight-bearing joints and the hands in a specific distribution.
When radiographic findings of OA are seen in younger patietns or in unusual locations, such as the shoulder, elbow, or ankle, then there is usually a predisposing prior trauma or other underlying arthritis.
The radiographic hallmarks of OA, regardless of location in the body, include:
Asymmetrical joint space narrowing.
Sclerosis of subchondral bone, stimulated by loss of hyaline cartilage and reactive remodeling.
Osteophytosis.
Subchondral cystic change, due to herniation of joint fluid into bone through a cartilage defect.
Lack of periarticular osteopenia.
Although joint space narrowing is present in all arthritides, osteoarthritis can be diagnosed with confidence when subchondral sclerosis, osteophytosis, and subchondral cystic changes are present and inflammatory erosions are absent.
When extensive subchondral cystic changes are present, calcium pyrophostae dihydrate crystal deposition disease (CPPD) should be considered as well.
Osteoarthritis in the hand
Similar to osteoarthritis of other joints, the radiographic hallmarks of OA in the hand include cartilage space narrowing, subchondral sclerosis, and osteophystosis. Erosions are absent.
In order of decreasing involvement, typical sites of OA is the hand include the distal interphalangeal joints (DIPs), the base of the thumb at the first carpometacarpal joint (CMC), and the proximal interphalangeal joints (PIPs).
The most common site of osteoarthritis in the hands is the second DIP.
Unlike rheumatoid arthritis, the metacarpophalangeal joints (MCPs) are less commonly affected.
Large osteophytes cause characteristic soft-tissue swelling surrounding the finger joints.
A Heberden node is a soft-tissue swelling around the DIP.
A Bouchard node is soft-tissue swelling around the PIP.
Osteoarthritis in the shoulder
The Grashey view (obtained posterioly in 40-degree obliqued external rotation) shows the glenohumeral joint in profile and best demonstrates cartilage space narrowing.
Osteoarthritis in the foot
The most common joint affected by OA in the foot is the metatarsophalgeal join (MTP) of the great toe, which may lead to hallux rigidus (a stiff big toe) from dorsal osteophytes.
Osteoarthritis also affects the talonavicular joint and is a cause of dorsal beaking.
Osteoarthritis in the knee
There are three joint compartments in the knee: the medial and lateral tibiofemoral compartments and the patellofemoral compartment. The typical pattern for OA of the knee is asymmetrical involvement of the medial tibiofemoral compartment. Severe osteoarthritis can involved all three compartments.
The following rule of thumb applies to OA in general, but especially in the knee: Osteophytes determine whether OA is present. The degree of joint space narrowing determines the severity of OA.
The degree of tibiofemoral cartilage space narrowing is best determined on standing weight-bearing veiws, often on standing films in flexion.
Bilateral involvement of the knees is typical.
Osteoarthritis in the hip
Similar to the knee, the involvement of hip oteoarthritis tends to be bilateral.
In addition to the typical features of OA including joint space narrowing, osteophytosis, subchondral cystic change, and sclerosis, hip OA also features characteristic migration of the femoral head in a superolateral direction. Less commonly, medial migration can be seen in hip OA.
In contrast, axial migration is seen more commonly in inflammatory arthritis.
Degenerative change in the spine
The vertebral body-disc articulations are cartilaginous joints. Vertebral body endplates are covered by hyaline cartilage that is anaolgous to articular cartilage in other joints. The intervertebral disk is composed of three components: The annulus fibrosus, nucleus pulposus, and the cartilaginous endplates.
Osteoarthritis only affects synovial joints. Therefore, in the spine, osteoarthritis can occur at the facet (zygapophyseal), atlantoaxial, uncovertebral joints ( in the cervical spine at C3-C7), costovertebral, and sacroiliac joints.
The spectrum of intervertebral disk degeneration is best described as degenerative disk disease (DDD), which is characterized by dessication of the intervertebral discs, endplate sclerosis, and osteophytosis.
Gas in the intervertebral disc, also called vacuum phenomenon, is commonly seen and is pathognomonic for degenerative disease. It is important not to confuse vacuum phenomenon (gas in intervertebral disc) with Kummmel disease, which is gas in a vertebral body compression fracture representing osteonecrosis.
Complications of DDD include spinal stenosis, neural foraminal stenosis, and degenerative spondylolisthesis.
Diffuse idiopathic skeletal hyperostosis (DISH) is a distinct entity from degenerative disc disease, but appears similar due to exuberant osteophytosis. DISH is defined as flowing bridging anterior osteophytes spanning at least four vertebral levels, with normal disk spaces and sacroiliac joints. The etiology of DISH is unknown. It is usually asymptomatic but may be a cause of dysphagia when it affects the cervical spine. DISH occurs in elderly patients. DISH is associated with ossification of the posterior longitudinal ligament (OPLL), which may be a cause of spinal stenosis. OPLL may be difficult to identify on MRI and is best seen on CT.
Osteoarthritis in the sacroiliac joint
Only the inferior portion of the sacroiliac joint is a synovial (diarthrodial) joint. The superior portion is a syndesmotic joint.
The typical changes of OA are only seen in the inferior (synovial) portion of the SI joint.
Overview of erosive osteoarthritis
Erosive osteoarthritis combines the clinical findings of rheumatoid arthritis (e.g. swelling) with imaging findins and distribution that are more similar to osteoarthritis.
Erosive OA typically affects elderly females.
Erosive osteoarthritis of the hands
The distribution of erosive osteoarthritis is limited to the hands, where the distribution is the same as degenerative OA (DIPs, CMC of the thumb, and PIPs).
Erosive OA features a characteristic gull-wing appearance of the DIP joint due to central erosion and marginal osteophytes.
Overview of rheumatoid arthritis
Rheumatoid arthritis (RA) is an autoimmune disorder where the synovium is the target of a waxing and waning immune response. Rheumatoid factor (RF) is typically positive, although it is not specific. RF is an antibody directed against IgG, which activates the complement cascade. RA clinically presents with symmetrical joint pain, swelling, and morning stiffness.
RA first affects the small joints in the hands and wrists. Foot involvement may occur early, so foot radiographs are routinely obtained in suspected cases of RA. In more advanced cases, RA affects the cervical spine, knees, shoulders, and hips.
The radiographic hallmarks of RA include:
Marginal erosions, which first occur at the intracapsular margins in the “bare area”. The bare area is a region of exposed bone just within the joint capsule that is not covered by thick cartilage.
Soft-tissue swelling.
Diffuse, symmetric joint space narrowing
Periarticular osteopenia.
Joint subluxation.
Rheumatoid arthritis in the hand and wrist
The hands are commonly affected in patients with RA.
Typical joints involved are the MCPs, PIPs, and the carpal articulations. The DIPs are usually spared.
The earliest radiographic chnages of RA are soft-tissue swelling and periarticular osteopenia, reflecting synovitis and hyperemia.
Erosions occur early in disease, typically of the radial aspects of the second and third metacarpal heads, the radial and ulnar aspects of the bases of the proximal phalanges, and the ulnar styloid.
Joint subluxations are present in more advanced disease, which typically are not reducible and lead to several common deformities, including: Boutonniere deforemity (PIP flexion and DIP hyperextension). Swan neck deformity (PIP hyperextension and DIP flexion). Ulnar subluxation of the fingers at the MCP.
Late-stage rheumatoid arthritis may uncommonly cause ankylosis (fibro-osseous joint fusion occuring after complete cartilage loss) of the wrist. Juvenile idiopathic arthritis (discussed later), in contrast, has a higher propensity for carpal ankylosis.
Rheumatoid arthritis in the feet
The feet are commonly involved in RA. Typically, the metatarsophalangeal (MTP) joints in the forefoot and the talocalcaneonavicular joint in the midfoot are involved. Up to 20% of patients have the MTP joint as the first site of involvement.
Rheumatoid arthritis in the hip
RA causes concentric cartilage loss, leading to axial migration of the femoral head. In contrast, osteoarthritis more commonly causes superior acetabular cartilage space narrowing and superolateral femoral head migration.
In severe cases, RA may cause a protrusio deformity, which is defined as > 3 mm medial deviation of the femoral head beyond the ilioischial line in males and >6 mm in females.
Rheumatoid arthritis in the knee
All three joint spaces (medial and lateral tibiofemoral and patellofemoral) may be affected by RA in the knee. In contrast, OA tends to first affect the medial tibiofemoral articulation. If osteophytes and symmetrical cartilage space narrowing are present, then secondary osteoarthritis should be considered.
Unlike the smaller joints affected by rheumatoid arthritis, erosions are not a prominent manifestation of rheumatoid arthritis of the knee.
Rheumatoid arthritis in the spine
The cervical spine is involved in up to 70% of patients. Involvement is increased with more severe and long-standing disease. The thoracic and lumbar spine are almost never involved.
The general pattern of rheumatoid arthritis in the cervical spine includes subluxation at multiple levels, osteopenia, and erosions of the odontoid, facet joints, vertebral endplates, and spinous processes. Unlike osteoarthritis, there is no bone production.
A characteristic finding of rheumatoid arthritis is atlantoaxial (C1-C2) subluxation. Atlantoaxial subluxation may occur in multiple directions, including anterior (most common), posterior, vertical (atlantoaxial impaction), rotatory, and lateral.
Anterior atlantoaxial subluxation is caused by inflammation of adjacent bursa and resultant laxity of the transverse ligament. Anterior atlantoaxial subluxation may not be apparent if flexion radiographs are not obtained. Anterior atlantoaxial subluxation is present if the atlanto-dental interval (ADI) is >2.5 mm (>5 mm in children). The atlanto-dental interval is the distance between the anterior aspect of the dens and the posterior aspect of the anterior ring of C1, as measured at the inferior aspect of the C1-C2 articulation.
Vertical atlantoaxial subluxation (also called atlantoaxial impaction) results from C1-C2 facet erosion and collapse, leading to protrusion of the odontoid through the foremen magnum. This may compress the midbrain. Direct visualization of the odontoid is usually not possible on a lateral radiograph, but impaction may cause the anterior arch of C1 (normally in line with the odontoid) to sink to the level of the body of C2.
In the setting of RA, posterior atlantoaxial subluxation is usually due to odontoid erosion. It may also be caused by odontoid fracture.
Rheumatoid arthritis in the shoulder
Rheumatoid arthritis causes chronic rotator cuff tears leading to the classic high riding humerus.
Erosions tend to occur in the lateral aspect of the humeral heads. At the acromioclavicular (AC) joints, erosion may lead to “penciling” of the distal clavicle.
Rheumatoid arthritis in the elbow
Rheumatoid arthritis involves the elbow in approximately one third of patients.
Overview of seronegative spondyloarthropathies
The seronegative spondyloarthropathies are a group of four inflammatory arthropathies, which by definition have negative rheumatoid factor. Patients are usually HLA-B27 positive.
The four seronegative spondyloarthopathies are ankylosing spondylitis, psoriatic arthritis, reactive arthritis (previously called Reiters arthropathy), and inflammatory bowel disease (IBD) associated arthropathy.
Sacroilitis is a hallmark of the spondyloarthopathies
Similar to involvement in OA, only the inferior aspect of the sacroiliac (SI) joint is affected in seronegative spondyloarthropathies because only the inferior portion is a synovial (diarthrodial) joint. Erosions first involve the iliac aspect of the SI joint.
Symmetric sacroilitis is caused by IBD and ankylosing spondylitis (mnemonic: both start with vowels).
Asymmetric sacroilitis is caused by psoriatic arthritis and reactive arthopathy (mnemonic: both start with consonants)
An important cause of unilateral sacroilitis is septic arthritis, especially in an immunocompromised patient or with intravenous drug abuse. Septic arthritis usually presents with erosive changes in a patient with fever and SI joint pain.
Inflammatory bowel disease
Sacroilitis associated with inflammatory bowel disease can be seen in patients with ulcerative colitis, Crohn disease, Whipple disease, and status post gastric bypass.
IBD-associated sacroilitis is typically symmetrical.
Ankylosing spondylitis
Ankylosing spondylitis (AS) is predominantly seen in young men with HLA-B27 and presents with back pain and stiffness. AS can be associated with pulmonary fibrosis (upper lobe predominant), aortitis, and cardiac conduction defects.
The earliest radiographic signs of AS are symmetric erosions, widening, and sclerosis of the sacroiliac joints.
Subsequently, the spine invariably becomes involved, with radiographic findings following a specific sequence, which ascends from the lumbar to the cervical spine.
Romanus lesions are erosions of the anterior spine or inferior edges of the vertebral body endplates caused by enthesitis (inflammation at a ligament or tendon insertion site) at attachment of the annulus fibrosus to the vertebral body.
Shiny corners represent sclerosis of prior Romanus lesions at the corners of the vertebral bodies.
Squaring of the vertebral body disc margins develops due to erosions and bone loss.
Delicate syndesmophytes represents bony bridging connecting adjacent vertebral margins, which create the classic bamboo spine (spinal ankylosis) in late-stage disease.
In advanced disease, the fully ankylosed spine is at a very high risk of fracture with even minor trauma. CT is necessary for evaluation of even minimal trauma in a patient with advanced AS and pain after trauma.
An Andersson lesion is a pseudoarthosis occurring in a completely ankylosed spine.
Psoriatic arthritis
Psoriatic arthritis clinically presents as arthropathy in a patient with skin psoriasis. Psoriatic arthritis most commonly affects the hands. In contrast to RA, mineralization is preserved. Sacroilitis, when present, is usually asymmetric.
There are several patterns of psoriatic arthritis, including oligoarthritis, polyarthritis, spondyloarthropathy (producing bulky asymmetric bridging), and arthritis mutilans ( a severe form usually affecting the hands, less commonly the feet).
In the hands, the radiographic hallmark of psoriatic arthritis is diffuse soft-tissue swelling of an entire digit, producing the sausage digit. Pencil-in-cup erosions are also characteristic, most commonly affecting the DIPs. Although hand findings are usually bilateral, involvement tends to be asymmetric. The severe arthritis mutilans variant can cause marked deformity and telescoping digits, also known as the main-en-lorgnette (opera-glass hand) deformity. Additional findings in the hands include fluffy periostitis and ill-defined erosions of the joint margins.
In the foot, the great toe IP and MTP joints are most commonly affected. An ivory phalanx represents osteosclerosis and is relatively specific for psoriatic arthritis. Psoriatic arthritis produces a plantar calcaneal spur with periosteal reaction. In contrast, a degenerative calcaneal spur will not feature reactive new bone.
In the spine, psoriatic arthritis causes formation of coarse bony bridging (bulky lateral bony outgrowths), sometimes indistinguishable from reactive arthropathy.
Reactive arthropathy (previously called Reiter disease)
Reactive arthropathy is an inflammatory arthritis thought to be a sequela of infectious diarrhea, urethritis, or cervicitis. Sacroilitis is usually asymmetric, as in psoriatic arthritis.
Reactive arthropathy predominantly affects the feet, where it has a similar appearance to psoriatic arthritis. Initial radiographic findings include diffuse soft-tissue swelling, joint space loss, aggressive marginal erosions, and juxta-articular osteopenia. Bony mineralization is preserved in the later stage of disease.
In particular, the calcaneus is a common site of involvement with bony proliferative changes including erosions, enthesophytes, and fluffy periosteal reaction. The posterior-superior aspect of the calcaneus is a frequent site of erosion due to adjacent bursitis. There is often secondary Achilles tendinitis and thickening of the soft tissues.
In the hands, reactive arthropathy affects the interphalngeal joints and MTPs with erosions and diaphyseal periostitis.
Reactive arthropathy may affect the spine with formation of coarse bony bridging, which may be difficult to distinguish from psoriatic arthritis.
Systemic lupus erythematosus (SLE)
Joint abnormalities are seen in ~90% of patients with systemic lupus erythematosus (SLE). The key radiographic finding of SLE is reducible subluxations of the MCPs and PIPs. Alignment may appear normal on a PA view when the hands are compressed against the radiographic plate. Subluxations become apparent in the Norgaard (“ballcatcher’s” or “you’re in good hands with Allstate”) or oblique views when the hand is not contrained.
Jaccoud arthropathy
Jaccoud arthropathy was historically described as being secondary to recurrent rheumatic fever, but some authors feel that SLE and Jaccoud arthropathy are the same disease. Both entities share the same type III hypersensitivity mechanism and feature identical radiographic findings of reducible subluxations in the hand.
Scleroderma
Scleroderma is a systemic collagen vascular disease caused by collaged deposition in the skin and soft-tissues. The fingertips are affected first, with atrophy of the distal soft tissues. Acroosteolysis (resorption of the distal portion of the distal phalanges) is characteristic, especially if there is accompanying calcification. The differential for acroosteolysis includes:
Collagen vascular disease, including scleroderma.
Neuropathy.
Polyvinyl chloride exposure.
Thermal injury (burn or frostbite). In frostbite the thumb is usually spared because it is clenched in a fist.
Hyperparathyroidism, seen in conjunction with subperiosteal resorption.
Hajdu-Cheney, a rare autosomal dominant syndrome characterized by short stature, craniofacial changes, and progressive acroosteolysis.
Dystrophic soft tissue and periarticular calcifications are common in scleroderma, which causes tightening and fibrosis of the skin and often leads to joint contractures.
Polymyositis and dermatomyositis
Polymyositis and dermatomyositis are idiopathic conditions characterized by inflammation of muscle (polymyositis) or muscle and skin (dermatomyositis). Joint abnormalities are rare, although periarticular osteopenia may be present in these conditions.
The imaging hallmark of polymyositis and dermatomyositis is soft-tissue calcification. Intramuscular calcifications are most common, although subcutaneous calcifications may also be seen, similar to scleroderma.
Calcium hydroxyapatite deposition disease (HADD)
Also called calcific tendinitis, calcium hydroxyapatite deposition disease (HADD) causes crystals to be deposited in the periarticular tissues. Hydroxyapatite crystals typically do not deposit directly within the joints (the articular cartilage and synovium are spared), but instead amoprhous deposition of calcium forms within tendons.
The supraspinatus tendon in the rotator cuff is most commonly affected in the shoulder.
Calcific tendinitis of the prevertebral longus coli muscle may cause neck pain, odynophagia, fever, and prevertebral effusion, and may clinicaly mimic a prevertebral abscess.
An intra-articular variant seen in the shoulder, called Miwaukee shouler, leads to rapid destruction of the rotator cuff and glenohumeral joint.
Calcium pyrophosphate dihydrate deposition disease (CPPD)
Calcium pyrophosphate dihydrate deposition disease (CPPD) is an inflammatory arthropathy caused by intra-articular deposition of calcium pyrophosphate dihydrate crystals. Microscopically, the rhomboid crystals of CPPD are positively birefringent.
CPPD has been called the “great mimicker” of other arthropathies. Clinical manifestations of CPPD disease include pseudoosteoarthritis (common), pseudogout (10-20%), pseudorheumatoid (2-6%), pseudoneuropathic (<2%), and asymptomatic (10-20%). CPPD is rare in a patient under 50. Crystal deposition may be idiopathic or associated with hemocrhomatosis, hyperparathryoidism, and hypophosphatasia.
The hallmark radiographic fidning of CPPD disease is chondrocalcinosis, which is calcification of hyaline (articular) or fibro- (meniscal) cartilage. Radiographs of the knees, wrist, and pelvis (pubic symphysis) are nearly 100% sensitive for the detection of chondrocalcinosis.
In the wrist, chondrocalcinosis tends to affect the triangular fibrocartilage complex (TFCC). Advanced disease may lead to scapholunate advanced collapse (SLAC) wrist. SLAC wrist is proximal migration of the capitate between the dissociated scaphoid and lunate, and may also be seen in RA or trauma.
In the knee, the patellofemoral compartment is affected first, but all three compartments may become involved. Isolated degenerative changes of the patellofemoral joint are highly suggestive of CPPD.
In the hands, involvement of the second and third MCP joints is typical, producing characteristic hook-like or drooping osteophytes from the radial aspect of the metacarpal heads. A similar appareance can be seen in hemochromatosis, which typically featrures more extensive involvement of the MCPs.
Gout
Gout is a crystal-induced inflammatory arthropathy caused by sodium urate deposition in the joints. Excess uric acid may be secondary to under-excretion (more common, typically caused by renal insufficiency) or overproduction (much more rare, typically seen in younger patients). It takes about 10-20 years of hyperuricemia before the clinical syndrome of gout develops. Microscopically, gout crystals are negatively birefringent needle-like crystals within neutrophils.
The great toe is most commonly involved, but gout can occur in any joint.
Radiographic hallmarks are sharply marginated erosions are sharply marginated erosions with overhanging margins, associated with soft-tissue gouty tophi.
Joint spaces are typically well preserved until late in the disease. Bony mineralization is preserved.
Hemochromatosis
Hemochromatosis arthropathy affects 50% of those with hemochromatosis, an autosomal recessive disease of altered iron metabolism. The arthropathy is caused by deposition of iron and calcium pyrophosphate dihydrate crystals. Hemochromatosis clinically presents with bronze pigmentation, diabetes, cirrhosis, cognestive heart failure, and arthropathy.
In the hand, the typical location of hemochromatosis arthropathy is the MCP joints, producing characteristic hook-like osteophytes at the metacarpal heads. Calcium pyrophosphate dihydrate deposition disease (CPPD) can appear identical when involvement is isolated to the 2nd and 3rd MCPs. In contrast to CPPD, hemochromatosis may involve all MCPs.
Acromegaly
Acromegaly (excess growth hormone) causes arthropathy due to enlargement of the articular cartilage and subsequent degeneration. In contrast to all other arthropathies, joint spaces are widened in early disease due to cartilage hypertrophy. Later in disease, secondary osteoarthritis occurs with cartilage space narrowing.
In the hand, beak-like osteophytes of the metacarpal heasd and spade-like enlargement of the terminal tufts are characteristic.
Amyloid arthropathy
Amyloid arthropathy is a rare noninflammatory arthropathy due to infiltration of bones, joints, and soft tissues by beta-pleated sheets of amino acids. Primary systemic amyloidosis is associated with monoclonal plasma cell dyscrasia. Secondary amyloidosis is associated with chronic underlying inflammation or infection. Another form of amyloidosis is caused by ß2-microglobulin accumulation in patients on chronic emodialysis.
A characteristic clinical finding of amyloidosis is bulky soft-tissue nodules in the shoulder superimposed upon atrophic shoulder muscles, producing the shoulder-pad sign.
Imaging findigns of amyloid arthopathy are nonspecific but may resemble RA. Intra-articular deposits cause articular cartilage destruction. Soft-tissue nodules and erosions may be present.
Ochronosis (alkaptonuria)
Ochronosis is the connective tissue manifestation of alkaptonuria. Alkaptonuria is caused by a defect in homogentisic acid oxidase, causing homogentisic acid polymers to accumulate in the visceral organs, intervertebral discs, and joints. Clinically homogentisic acid in the urine turns black when exposed to air.
A specific finding of ochronosis is intervertebral disc calcifications at every level with accompanying disk space narrowing.
Multicentric reticulohistocytosis
Multicentric reticulohistiocytosis is a rare disease where lipid-laden macrophages are deposited in soft tissues and periarticular tendons, forming skin nodules and erosions with sclerotic margins.
The well-defined erosions of multicentric reticulohistiocytosis tend to affect the DIPs symmetrically. Other radiographic findings of multicentric reticulohistiocytosis include soft-tissue nodules and preserved bone density.
Joint destruction may be rapid and progressive, producing an arthritis mutilans appearance.
Hemophilic arthropathy
Hemophilia is an X-linked inherited disorder of either factor VIII (Hemophilia A) or IX (hemophilia B; christmas disease) deficiency causing recurrent bleeding.
Hemophilia most often affects the knees, elbows, and ankles. Recurrent hemarthrosis results in synovial hypertrophy and hyperemia. The hyperemia may cause epiphyseal enlargement and early fusion.
Characteristic appearance of the elbow is an enlarged radial head and widened trochlear notch. Characteristic appearance of the knee is squaringof the patella and widened intercondylar notch.
Secondary arthritis may lead to marked joint space narrowing.
Deposition of iron in the synovium causes increased soft-tissue density around joints.
Juvenile idiopathic arthritis also causes articular hyperemia and may have similar radiographic findings, especially in the knee (widened intercondylar notch) and elbow (enlarged radial head).
Pseudotumor of hemophilia is a benign lesion caused by recurrent intraosseous or subperiosteal bleeding. The chronic cyclical bleeding leads to bony scalloping and pressure erosion, often with an associated soft-tissue mass.
On radiography, pseudotumor is benign-appearing, with well-circumscribed and sclerotic margins. Pseudotumor may have a complex MRI appearance due to different stages of blood products.
Juvenile Idiopathic arthritis (JIA), previously called juvenile rhematoid arthritis
Juvenile idiopathic arthritis (JIA) is a spectrum of related chronic inflammatory arthropathies affecting children under 16 years of age.
Monoarticular or pauciarticular (most common) JIA may affect either a single joint or a few joints including the knees, ankles, elbows, or wrists.
Polyarticular JIA is a systemic disease affecting multiple joints including the hands, feet, and cervical spine in addition to the joints affected by mono-pauciarticular disease.
A variant of JIA is Still disease, which is a systemic disorder affecting children younger than 5, featuring acute febrile illness, rash, adenopathy, pericarditis, and mild arthralgias.
Radiographic hallmarks of JIA are abnormal bone length or morphology due to hyperemia in a skeletally immature patient. Growth disturbances are more commonly seen in early onset disease. Abnormal morphology results from epiphyseal overgrowth and enlargement (ballooning) of the ends of bone. Affected joints demonstrate premature skeletal maturation and physeal fusion.
In the hand, premature fusion of the growth plate may cause brachydactyly.
In the knee, the characteristic appearance is a widened intercondylar notch, metaphyseal flaring, and uniform joint space narrowing. This appearance can be similar to hemophilia.
In the elbow, there is characteristic enlargement of the radial head and trochlear notch, with uniform cartilage space narrowing. These findings can also be seen in hemophilia.
In the hips, symmetrical cartilage space narrowing, protrusio deformity, and gracile appearance of the femoral shaft are characteristic.
Akylosis may occur in the wrist and zygapophyseal (facet) joints of the cervical spine. Ankylosis occurs more commonly in juvenile idiopathic arthopathy compared to adult rheumatoid arthritis. The differential diagnosis of a child with cervical spine ankylosis is Klippel-Feil syndrome, which is failure of cervical segmentation.
Neuropathic arthropathy (Charcot joint)
Neuropathic arthropathy, also called Charcot joint, is a destructive form of arthritis caused by neurosensory deficit. Lack of sensation ultimately causes severe degenerative changes with fragmentation of bone and cartilage.
Neuropathic arthropathy clinically presents as a (usually) painless, swollen joint. The peripheral neuropathy of diabetes is implicated most frequently, typically affecting joints in the ankle and foot. Other causes include syringomyelia (usually affecting the upper extremity), chronic alcohol abuse, amyloid, spinal tumors, and very rarely syphilis or leprosy.
Two forms of neuropathic arthropathy are hypertrophic (more common) and atrophic variants.
The hypertrophic variant looks like anarchy in a joint, with destruction, dislocation (or subluxation), debris, disorganization, and no demineralization.
The atrophic variant of neuropathic arthropathy occurs most commonly in the shoulder. It features a classic radiographic appearance of humeral head resorption with a sharp, surgical-like margin. Syringomyelia should be suspected in upper extremity neuropathic arthropathy and confirmed by cervical spine MRI.
Sarcoidosis
Sarcoidosis is a multisystemic granulomatous disease. Lung findings, including adenopathy and parenchymal disease, are present in the majority of patients and are the primary manifestations of disease.
Bony manifestations of sarcoid are rare. A characteristic finding in the hands is lace-like lytic lesions in the middle or distal phalanges.
Sarcoidosis may also manifest as acute or chronic polyarthritis, although there areno distinctive radiographic patterns. Ankle invovlement, especially if bilateral or associated with erythema nodosum, should raise suspicion of sarcoidosis and prompt a chest radiograph.
Evaluation of the hands for arthritis: ABCDEs
Alignment
Bone mineral density
Bone creation
Calcification
Cartilage spaces
Distribution
Erosions
Soft-tissue swelling
Arthritis alignment
Subluxations - Non-reducible subluxations are seen in rheumatoid arthritis. Reducible subluxations are typical for systemic lupus erythematosus (SLE) or Jaccoud arthropathy. In contrast to rheumatoid, erosions are not typically seen in SLE.
Dislocations - Joint dislocations may be present in advanced rheumatoid arthritis.
Arthritis bone mineral density
Evaluation of bone mineral density - Bone mineral density is evaluated by assessing the cortical thickness of the second metacarpal shaft. The cortical thickness should be at least 1/3 of the total width of the metacarpal shaft. Evaluation of bone density helps to distinguish betwen inflammatory and non-inlfammatory arthropathies.
Diffuse osteopenia - Diffuse osteopenia is associated with advanced rheumatoid arthritis. Note that generalized osteoporosis secondary to a medical condition can be seen in any arthropathy.
Periarticular osteopenia - Periarticular osteopenia is a nonspecific finding that can be seen in rheumatoid arthritis or the early stage of any inflammatory arthropathy.
Arthritis bone creation
Osteophytosis - An osteophyte is the result of endochondral bone formation that occurs at the margins of a joint and is caused by degeneration of the adjacent articular cartilage. Osteophyte formation is the hallmark of osteoarthritis but can also be seen as a secondary finding in other conditions such as CPPD and hemochromatosis.
Periosteal new bone - Periosteal new bone formation may be triggered as a reparative response to erosive change. Periosteal reaction is seen in psoriatic arthritis and reactive arthropathy, but is less common in adult rheumatoid arthritis.
Bony ankylosis - Ankylosis is the bony fusion of a joint and is seen in aggressive arthropathies that destroy articular cartilage.
Akylosis of the wrist and cervical spine is a typical finding in advanced juvenile idiopathic arthropathy. In advanced rheumatoid arthritis, akylosis may uncommonly occur in the wrists.
Ankylosis of the DIPs is a typical finding in some cases of psoriatic arthritis.
Arthritis Calcification
Crystal deposition diseases known to cause arthritis are calcium pyrophosphate dihydrate (CPPD) deposition disease, hydroxyapatite deposition disease (HADD), and sodium urate monohydrate arthropathy (gout)
Chondrocalcinosis - chondrocalcinosis is typically due to deposition of calcium pyrophosphate dihydrate crystals in cartilage, which may be idiopathic or due to hyperparathyroidism or hemochromatosis.
Calcification of tendons - Calcification of tendons is typically caused by deposition of hydroxyapatite crystals, and is also known as calcific tendinitis. Tendon calcification can also been seen in CPPD.
The radiolucent urate crystals that make up a gouty tophus may precipitate calcium. Soft tissue calcifications can also be seen in scleroderma, dermatomyositis, polymyositis, and SLE.
Arthritis Cartilage Spaces
Preserved cartilage spaces - Gout generally features preserved cartilage spaces. Focal narrowing may be present in the region of the gouty tophi and erosion.
Asymmetrical narrowing - Asymmetrical cartilage space narrowing is typical of osteoarthritis and gout.
Symmetrical narrowing - Symmetrical cartilage space narrowing is seen in the inflammatory arthropathies.
Increased cartilage spaces - Acromegaly produces cartilae space widening early in the disease, prior to the development of secondary osteoarthritis.
Arthritis Distribution
Hand: DIP and PIP - Osteophytes present: Osteoarthritis (no erosions); erosive osteoarthritis (erosions present). No osteophytes: Psoriatic arthritis (erosions present).
Hand: MCP and PIP - Without new bone formation: Rheumatoid arthritis
Hand: MCP only - With erosions: Rheumatoid arthritis. With osteophytes: CPPD or hemochromatosis.
Wrist: CMC - Osteophytes without erosions: Osteoarthritis. Osteophytes with erosions: Erosive osteoarthritis.
Erosions without osteophytes: Gout.
Wrist: diffuse (pan-carpal) - Inflammatory arthropathy. Post-traumatic osteoarthritis can occur anywhere in the wrist.
Arthritis Erosions
Erosions are first seen in the “bare” are of bone just inside the joint at the edge of attachment of synovium. Erosions may subsequently spread further into the joint and even destroy the entire joint in severe cases.
Variable erosions - Rheumatoid arthritis may feature erosions in certain characteristic locations, including the radial aspect of the second and third metacarpal heads, the bases of the proximal phalanges, and the ulnar styloid.
Pencil in cup erosion - Psoriatic arthritis.
Gullwing erosions - Erosive osteoarthritis.
Overhanging margin of cortex - Gout. Caused by chronic erosion from a tophus remodeling in the cortex.
Arthritis Soft tissue swelling
Symmetrical swelling around a joint - A characteristic finding of rheumatoid arthritis is joint distention, which radiographically appears as soft-tissue swelling, although this finding can be seen in any inflammatory arthropathy.
Asymmetrical swelling around a joint - In osteoarthritis, characteristic locations of nodular soft-tissue swelling are due to osteophytes and capsul-ligamentous thickening. Heberden node: swelling of the DIP. Bouchard node: Swelling of the PIP.
Swelling of an entire digit - “Sausage digit” in the hand: Psoriatic arthritis or reactive arthopathy. “Sausage digit” in the foot: More commonly reactive arthropathy.
Lumpy-bumpy soft-tissue swelling - Lumpy-bumpy soft-tissue swelling is typically caused by infiltration with a foreign substance, such as gouty tophi, sarcoidosis, amyloid, or multicentric reticulohistiocytosis.
Bone tumor and tumor-like lesion morphology
Periosteal reaction - The morphology of a bone lesion’s associated periosteal reaction gives an important clue to the rate of growth, and hence the aggressiveness, of the lesion.
Pattern of bone destruction: Margin analysis - Analysis of a bone lesion’s margins (i.e., zone of transition from normal to abnormal bone) helps to characterize the bony destruction and stratify a lesion as aggressive or non-aggressive. A sharply marginated zone of transition usually denotes a less aggressive lesion with slower rate of growth. The faster the rate of growth, the more aggressive the lesion may be. A wide zone of transition suggests rapid growth and a more aggressive lesion.
New matrix created by tumor - Matrix produced by an osteoid lesion, such as malignant osteosarcoma, appears as fluffy, cloud-like bone. Matrix produced by a chondroid lesion, such as a benign enchondroma or malignant chondrosarcoma, has a ring and arc or popcorn-like appearance. A ground glass matrix describes blurring of the trabeculae and is seen in fibrous dysplasia, a benign fibroosseous lesion involving abnormal proliferation of intraosseous fibroblasts.
Unique features - The fallen-fragment sign is seen in a simple (unicameral) bone cyst with pathologic fracture. An aneurysmal or expansile appearance suggests an aneurysmal bone cyst. Resorption of distal clavicles or tumoral calcinosis can suggest hyperparathyroidism, which can cause brown tumors.
Lodwick classification of bone destruction
The Lodwick classification of bone destructio helps to stratify aggressiveness:
Type 1: Geographic pattern: Margins have a thin zone of transition and may be sclerotic or well-defined.
1A: Think sclerotic margins. Almost always non-aggressive.
1B: Well-defined margins. Usually non-aggressive.
1C: Any part of the margin is indistinct.
Type 2: Moth-eaten pattern: It is difficult to define any border at all. Agressive
Type 3: Permeative: The permeative pattern is characterized by multiple tiny holes that infiltrate the bone. The pattern is very aggressive and is seen in lymphoma, leukemia, and Ewing sarcoma.
Bone tumor patient age
The two most likely considerations of an aggressive lytic bone lesion in a patient over age 40 are metastasis or myeloma.
Under age 20, an aggressive lytic lesion is most likely to represent eosinophilic granuloma, infection, or Ewing sarcoma.
Bone tumor location within bone
Eccentric within bone - Giant-cell tumor, chondroblastoma, aneurysmal bone cyst, non-ossifying fibroma, and the rare chondromyxoid fibroma are located eccentrically within the bone.
Central (in the middle of a long bone) - Simple bone cyst, enchondroma, and fibrous dysplasia are located centrally within the bone.
Benign and incidental: Enostosis (bone island)
Enostosis (commonly called a bone island) is an extremely common incidental finding of a small spiculated osteoblastic focus.
A bone island is only clinically significant in that it may rarely be difficult to differentiate from an osteoblastic metastasis, osteoid osteoma, or a low-grade osteosarcoma.
A giant variant ( >2 cm) may be most difficult to differentiate from low-grade osteosarcoma.
Bone scan of bone island is usually normal.
Osteopoikolosis is an autosomal dominant syndrome of multiple bone islands and keloid formation.
Osteopathia striata is a benign, asymptomatic sclerotic dysplasia characterized by linear bands of sclerosis in the long bones and fan-like sclerosis in the flat pelvic bones. Bone scan is typically normal.
Benign and incidental: Osteoma
Osteoma is a slow-growing lesion that may arise from the cortex of the skull or the frontal/ethmoid sinuses.
Gardner syndrome is an autosomal dominant syndrome of multiple osteomas, intestinal polyposis, and soft-tissue desmoid tumors.
In contrast to a bone island, osteoma arises from the cortex rather than the medullary canal.
Benign: Melorheostosis
Melorheostosis (also commonly spelled melorrheostosis) is a non-neoplastic proliferation of thickened and irregular cortex with a typical candle-wax appearance.
It clinically presents with pain, decreased range of motion, leg-bowing, and leg-length descrepancy.
Melorheostosis may be associated with scleroderma-like skin lesions over the affected region.
Melorheostosis is usually seen in a single lower limb, in the distribution of a single sclerotome. A sclerotome represents a zone supplied by a single sensory nerve.
Melorheostosis features intense uptake on bone scan.
Benign: Osteoid osteoma
Osteoid osteoma is a benign osteoblastic lesion characterized by a nidus of osteoid tisue surrounded by reactive bone sclerosis. The etiology is controversial. Inflammatory, vascular, and viral causes have been proposed.
The classic clinical presentation is night pain relieved by aspirin in a teenager or young adult.
Osteoid osteoma tends to occur in the diaphyses of the leg long bones (femur and tibia) most commonly. About 20% occur in the posterior elements of the spine. Spinal osteoid osteoma is an important cause of painful scoliosis.
On radiography and CT, a lucent nidus is surrounded by sclerosis. There is often central calcification within the nidus. Bone scan will be positive, with the double density sign representing intense uptake centrally in the region of the nidus and adjacent reactive uptake corresponding to sclerosis. Osteoid osteoma can be difficult to see on MRI alone. The nidus is usually low-signal on T1-weighted images and reactive marrow edema can obscure the lesion on T2-weighted images.
Treatment of osteoid osteoma is interventional radiology radiofrequency ablation, surgical curettage, or resection.
Benign: Osteoblastoma
Osteoblastoma is a benign osteoid-producing tumor that is histologically the same as an osteoid osteoma but is greater than 2 cm in size.
Osteoblastoma is approximately four times less common than osteoid osteoma, although it also occurs in the adolescent/young adult age range and also presents with pain. Interestingly, the pain of osteoblastoma is not typically relieved by aspirin.
The most common location is the posterior elements of the spine, occurring anywhere from the cervical spine through the sacrum. Osteoblastoma may also occur in the femur and tibia.
The most common location is the posterior elements of the spine, occurring anywhere from the cervical spine through the sacrum. Osteoblastoma may also occur in the femur and tibia.
The most common radiographic appearance of osteoblastoma is a lytic lesion with mineralization. Very rarely, osteoblastoma may be aggressive with a large soft-tissue mass, but lacking metastatic potential. Secondary aneurysmal bone cyst may be seen, especially when spinal in location.
A lytic lesion in the posterior elements of a young person may represent an osteoblastoma or aneurysmal bone cyst. If any mineralization is present within the lesion, osteoblastoma should be favored.
Malignant: Osteosarcoma
Osteosarcoma represents a heterogenous group of malignant tumors where the neoplastic cells are derived from osteoid lineage and most subtypes produce an osteoid matrix.
Osteosarcoma can be primary or secondary. Secondary osteosarcoma may arise from Paget disease or after radiation. Secondary osteosarcoma in Paget disease is extremely aggressive.
General imaging hallmarks of osteosarcoma are bony destruction, production of osteoid matrix, aggressive periosteal reaction, and an associated soft-tissue mass. Early osteosarcoma may be only evident as subtle sclerosis.
There are more than 10 primary subtypes. The four most important subtypes are conventional (most common), telangiectatic, and the two juxtacortical subtypes including parosteal (pronounced PAR-osteal) and periosteal.
Conventional (intramedullary) osteosarcoma represents 75% of osteosarcomas and occurs in adolescents/young adults usually around the knee in the metaphysis of the femur or tibia.
Telangiectatic osteosarcoma is an osteolytic destructive sarcoma, which may mimic a benign aneurysmal bone cyst on imaging. The presence of solid nodular components on MRI helps to differentiate a telangiectatic osteosarcoma from a benign aneursymal bone cyst. Unlike other osteosarcomas, telangiectatic osteosarcoma is vascular with large cystic spaces filled with blood. Although telangiectatic osteosarcoma is an aggressive lesion, new treatment options increase survival, which is now slightly improved compared to a conventional osteosarcoma.
Parosteal osteosarcoma is a juxtacortical osteosarcoma that arises from the outer periosteum. It most commonly occurs at the posterior aspect of distal femoral metaphysis and has a cauliflower-like exophytic morphology (mnemonic:par-boil cauliflower before eating). A lucent line may be seen separating it from the cortex. Patients are usually in their 3rd and 4th decades, older compared to other osteosarcoma subtypes. Parosteal osteosarcoma is the least malignant of all osteosarcomas, with ~90% 5-year survival.
Periosteal osteosarcoma, the other juxtacortical osteosarcoma, is a rare osteosarcoma variant arising from the inner periosteum. It features cortical thickening, aggressive periosteal reaction, and a soft-tissue mass. Histologically, periosteal osteosarcoma may show chondroid differentiation. The most common location of periosteal osteosarcoma is the diaphysis of the femur or tibia. Patients tend to be younger than 20 years old.
Regardless of subtype, osteosarcoma may metastastize to lungs, where the metastases typically calcify.
Benign: Synovial chondromatosis/osteochondromatosis
Synovial chondromatosis is non-neoplastic synovial metaplasia characterized by the formation of intra-articular lobulated cartilaginous nodules, which may or may not ossify. It is usually a monoarticular disorder.
The cartilaginous foci often ossify, in which case the term osteochondromatosis is used.
Synovial proliferation tends not to directly cause arthropathy, although the intra-articular nodules may cause mechanical erosions and secondary osteoarthritis.
The most common location is the knee. The shoulders, hip, and elbow may also be affected.
Radiography shows multiple round intra-articular bodies of similar size and variable mineralization. The primary differential is intra-articular bodies from osteoarthritis; however, in ostoearthritis the bodies tend to be more varied in size and shape and fewer in number. Diagnosis can be difficult in the absence of calcification, especially if mechanical erosions are present.
MRI appearances are variable, depending on the degree of ossification and the presence of chondroid matrix. When calcified or ossified, MRI will show multiple globular and rounded foci of low signal.
The MRI finding of multiple intra-articular low-intensity foci is nonspecific and can also be seen in pigmented villonodular synovitis (PVNS). A radiograph will clearly show rounded calcified bodies in osteochondromatosis.
Very rarely, malignant degenerate to chondrosarcoma may occur.
Benign: Enchondroma
Enchondroma is a benign lesion of mature hyaline cartilage rests.
In the long bones, enchondroma features characteristic chondroid (popcorn or ring and arc) calcifications.
The differential diagnosis of enchondroma includes medullary bone infarct (which produces serpetine sclerosis) and chondrosarcoma.
MRI is usually able to differentiate between infarct and enchondroma. Enchondroma has a characteristic lobulated hyperintense signal on T2-weighted images.
When occurring in the hand, enchondroma typically does not produce visible matrix and appears as a geographic lytic lesion.
Enchondroma may be complicated by pathologic fracture.
Enchondroma may rarely undergo malignant transformation. Aside from Ollier and Maffucci syndrome, malignant transformation to chondrosarcoma is very rare, with the key finding being new pain in the absence of fracture. Other findings suggestive of malignant transformation include: Soft-tissue mass. Destruction of the cortex. Thickening of the cortex.
Treatement of enchondroma is currettage.
Multiple enchondromas are seen in Ollier (multiple enchondromas only) and Maffucci (multiple enchondromas and venous malformations producing phleboliths) syndromes, the two familial enchondromatoses. Both syndromes carry an increased risk of malignant transformation to chondrosarcoma, with a higher risk in Maffucci syndrome.
Benign: Osteochondroma
An osteochondroma is a benign cartilage-capped bony growth projecting outward form bone, often pedunculated. It is the most common benign bone lesion.
Osteochondroma may present clinically as a palpable mass, which usually stops growing at skeletal maturity.
Key features are the continuity of cortex of host bone with the cortex of the osteochondroma and communication of the medullary cavities. Osteochondroma arises from the metaphysis and grows away from the epihysis.
An uncommon complication is malignant transformation to chondrosarcoma. Like enchondroma, the presence of pain in the absence of a pathologic fracture is a red flag. An associated soft-tissue mass is usually present with malignant transformation. A cartilage cap thickness >2 cm on MRI suggests malignant transformation to chondrosarcoma.
Multiple osteochondromas can be seen in familial osteochondromatosis (multiple hereditary exostoses), with increased risk for malignant transformation. Familial osteochondromatosis is an autosomal dominant skeletal dysplasia, with the knees most commonly involved.
Benign: Chondroblastoma
Chondroblastoma is a benign lesion located eccentrically in the epiphysis of a long bone in a skeletally immature patient. It is most commonly occurs about the knee or proximal humerus.
Calcified chondroid matrix is present on almost all CT studies, but is seen only ~50% of the time on radiographs.
Chondroblastoma is unique amongst chondroid lesions in that it typically demonstrates low or intermediate signal on T2-weighted images. Most chondroid lesions are T2 hyperintense.
Treatment is with curettage, cryosurgery, or radiofrequency ablation. There is a low risk of local recurrence. Chondroblastoma is very rarely malignant.
Benign: Chondromyxoid fibroma
Chondromyxoid fibroma is a very rare, benign cartilage tumor that is typically eccentric in the tibial or femoral metaphysis about the knee. It rarely demonstrates chondroid matrix.
It usually has sclerotic margins on radiography and is high in signal on T2-weighted MRI.
Malignant: Chondrosarcoma
Chondrosarcoma is a malignant tumor of cartilage. Like osteosarcoma, there are multiple primary and secondary variants.
Secondary forms arise from enchondroma (more commoly in the Maffucci and Ollier familial enchondromatoses), Paget disease, and osteochondroma (more common in familial osteochondromatosis). An osteochondroma with cartilage cap thickness of >2 cm is highly suggestive of chondrosarcoma.
The conventional (intramedullary) chondrosarcoma subtype is most common. On imaging, chondrosarcoma is typically an expansile lesion in the medullary bone, with ring and arc chondroid matrix. The tumor causes thickening and endosteal scalloping of the cortex, and there is often an associated soft-tissue mass.
The dedifferentiated subtype of chondrosarcoma is aggressive and may contain fibrosarcoma or osteosarcoma elements.
Other subtypes of chondrosarcoma include the rare mesenchymal and clear cell variants.
Benign: Nonossifying fibroma/fibrous cortical defect
Nonossifying fibroma (sometimes called a fibroxanthoma) is an asymptomatic and common incidental radiolucent lesion in the long bones (especially the leg) in children and adolescents. Nonossifying fibroma and fibrous cortical defect are thought to represent the same lesion; the term nonossifying fibroma is generally reserved for larger (>2 cm) or symptomatic lesions. They are the same histologically. These lesions are believed to arise from the periosteum.
The radiographic appearance is usually diagnostic and demonstrates a lucent lesion with a narrow zone of transition, sclerotic margin, and no matrix calcification. CT or MRI may show cortical disruption or thinning, representing replacement of the cortex by fibrous tissue.
Most lesions undergo spontaneous sclerotic involution as the patient reaches adulthood.
Malignant: Malignant fibrous histiocytoma (MFH)
Malignant fibrous histiocytoma (MFH) is a controversial waste-basket diagnosis more recently renamed as undifferentiated pleomorphic sarcoma not otherwise specified. Despite the controversy and recent renaming, the term MFH is still in common use by radiologists.
The term “fibrous” refers to the microscopy appearance of MFH, not to the cell of origin. In fact, no definite cell of origin has been determined.
MFH is the most common adult soft-tissue sarcoma. It usually occurs in middle-aged or older adults in the thigh or the retroperitoneum, but it may occur in any extremity. Less commonly, MFH may occur in the bone, where it appears as an aggressive, lytic lesion.
Fibrous dysplasia
Fibrous dysplasia is a benign congenital non-neoplastic condition of children and young adults characterized by replacement of normal cancellous bone by abnormal fibrous tissue.
Fibrous dysplasia can affect one bone (monostotic) or multiple bones (polyostotic). When polyostotic, it tends to be unilateral.
The most frequent complication is pathologic fracture, commonly at the femoral neck.
Fibrous dysplasia of the long bones tends to be central and metadiaphyseal, often causing a bowing deformity such as the extreme varus of the shepherd’s crook.
In the ribs or long bones, the matrix is typically indistinct and ground glass.
In the pelvic bones, fibrous dysplasia is often cystic.
In the skull base, fibrous dysplasia is typically expansile and can look highly unusual on MRI. The primary differential of an expansile skull base lesion is Paget disease, but the age of the patient is the key: fibrous dysplasia occurs in children and young adults, while Paget occurs in older adults.
McCune-Albright syndrome is polyostotic fibrous dysplasia, precocious puberty, and cutaneous café au lait spots.
Mazabraud syndrome is fibrous dysplasia and intramuscular myxomas, which tend to occur in the same region of the body.
Benign: Hemangioma
Hemangioma is a benign lesion that typically occurs in the vertebral body, characterized by vascular channels lined by endothelial cells.
Although usually incidental, rarely a hemangioma may be associated with a soft-tissue mass that can cause neurologic compromise.
Hemangioma causes reactive trabecular thickening in response to bony resorption by vascular channels.
On MRI, high signal intensity on both T1- and T2-weighted images from fat contained within the hemangioma. On radiography and CT, corduroy striations are typical. The polka-dot sign demonstrates thickened trabeculae imaged in cross-section.
Malignant: Angiosarcoma of bone
Angiosarcoma looks and acts aggrssively. Lung metastases are often seen.
(usually) benign: Giant cell tumor (osteoclasoma)
Giant cell tumor is an epiphyseal lucent lesion located eccentrically at the articular end of long bones in skeletally mature patients between ages 20 and 40. It arises from the metaphysis but crosses the closed epiphyseal plate to involve the epiphysis. The cell of origin is a multinucleated giant cell, similar in appearance to an osteoclast.
Most giant cell tumors are benign. Approximately 5% are malignant, but it is impossible to differentiate behavior based on the appearance of the primary lesion.
Multifocal giant cell tumors can be seen in Paget disease or hyperparathyroidism.
Treatment is typically curettage or wide resection.
Benign: Eosinophilic granuloma (Langerhans cell histiocytosis)
A disorder of immune regulation, Langerhans cell histiocytosis (LCH) is caused by an abnormal proliferation of histiocytes. LCH is primarily seen in children 5-10 years old and is discussed more in depth in the pediatric imaging section.
In the skull, the classic appearance of LCH is a lytic lesion with a beveled edge.
In the mdandible or maxilla, LCH may cause a floating tooth from resorption of alveolar bone.
In the spine, LCH may appear as a destructive radiolucent lesion with aggressive (often lamellated) periosteal reaction that may look like lymphoma or Ewing sarcoma.
Malignant: Ewing sarcoma
Ewing sarcoma is a highly malignant small round cell tumor (similar to PNET) affecting children and adolescents with a male predominance. The clinical presentation is nonspecific. Ewing sarcoma usually presents with pain. Systemic symptoms including fever are often present, making the distinction between Ewing sarcoma and osteomyelitis difficult.
Ewing sarcoma is the second most common pediatric primary bone tumor (following osteosarcoma).
Radiographic featrues are of an aggressive lesion, with permeative bone destruction, aggressive periosteal reaction, and often an associated soft-tissue mass.
In addition to Ewing sarcoma, the differential of an aggressive lytic lesion in a child includes osteomyelitis, eosinophilic granuloma, and metastatic neuroblastoma.
Malignant: Multiple myeloma (MM)/Plasmactyoma
Multiple myeloma is the most common primary malignant bone tumor in patients over 40.
By far the most common presentation of myeloma is multiple lytic lesions, with the most severe form being diffuse myelomatosis with endosteal scalloping.
Sclerosing myelomatosis is an uncommon variant, associated with POEMS syndrome: Polyneuropathy. Organomegaly (liver/spleen). Endocrine disturbances (amenorrhea/gynecomastia). Monoclonal gammopathy. Skin changes (hirsutism and hyperpigmentation).
The main differential of multiple lytic lesions in an adult is metastatic disease. Multiple myeloma originates from the red marrow and usually does not involve regions where there is minimal red marrow, such as the pedicles in th spine. Multiple myeloma may be negative on bone scan, unlike most metastases.
A solitary tumor is a plasmacytoma. Most patients with plasmacytoma will get full-blown multiple myeloma within 5 years.
Malignant: Lymphoma
Primary bone lymphoma is very rare and tends to ccur in adults over 40.
Bone lymphoma appears as an aggressive lytic lesion, but may also be an important differential consideration for an ivory (diffusely sclerotic) vertebral body.
Lymphoma is often associated with an adjacent soft-tissue mass.
Benign: Lipoma
Intraosseous lipoma is an uncommon benign neoplasm. The most common sites are the calcaneus, subtrochanteric region of the femur, distal tibial/fibula, and metatarsals. Imaging can be variable depending on the degree of fat, calcification, fibrous tissue, and peripheral sclerosis. Central or ring-like calcification is often present.
Soft-tissue lipoma is the most common soft-tissue tumor. It is important to note that up to one third of lipomas may contain nonadipose tissue. The presence of minimal nonadipose tissue does not suggest malignant transformation.
Malignant: Liposarcoma
The primary differential consideration of a soft-tissue lipoma containing nonadipose tissue is a well-differentiated liposarcoma, also called an atypical lipoma.
Features suggesting well-differentiated liposarcoma include large size (>10 cm), thick septations, globular or nodular soft tissue, or a composition consisting of <75% fat.
Malignant: Chordoma
Chordoma is a malignant lesion deriving from a notochord remnant. It arises in the midline of the axial skeleton, either in the spheno-occipital region, body of C2, or sacrococcygeal location.
Chordoma is a highly destructive lesion with irregular borders.
Calcifications may be seen within the lesion. These calcifications are due to necrosis, not bone formation.
Benign: Simple bone cyst (SBC), also called unicameral bone cyst (UBC)
Simple bone cyst/unicameral bone cyst is the result of a benign local disturbance of bone growth in children and adolescents.
The lesion is either hollow or fluid filled and typically found in the proximal diaphysis of the humerus or femur. Other locations include the calcaneus, iliac bone, and tibia.
SBC lacks periosteal reaction (in contrast to aneurysmal bone cyst), as long as there is no fracture.
Up to 66% of cases are complicated by pathologic fracture. The fallen fragment sign represents a cortical fragment that has fellen into the cyst. It is pathognomonic for SBC when seen in a young patient in a lesion in an appropriate location for SBC.
SBC is always located centrally within a bone.
Fluid-fluid levels are seen on MRI. Fluid levels are nonspecific and can also be seen in aneursymal bone cyst, giant cell tumor, and telangiectatic osteosarcoma.
One nonsurgical treatment option is the intra-lesional injection of methylprednisolone, which induces osteogenesis.
Benign: Aneurysmal bone cyst (ABC)
Aneurysmal bone cyst (ABC) is an expansile or “aneurysmal” multicystic lesion seen in children and adolescents.
Histologically, ABC is made of blood-filled sinusoids and solid fibrous elements. ABC may arise secondarily within a pre-existing tumor. This is important to consider if an aggressive lesion is biopsied and the pathology returns ABC, as this may imply that the true lesion was not sampled.
Unlike SBC, ABC can be located anywhere in bone (central or eccentric). It may occur in the posterior elements of the spine. Unlike SBC, ABC often features a “buttressing” smooth periosteal reaction at the proximal and distal aspects. Like SBC, fluid levels are present.
Malignant: Adamantinoma
Adamantinoma is a very rare, low-grade malignant tumor occurring in the tibia with a soap-bubble appearance. It may be difficult to differentiate from fibrous dysplasia.
Osseous metastasis
Osseous metastases are over ten times more common than primary bone tumors.
Most metastases occur in the red bone marrow, most commonly in the axial skeleton.
It can be difficult to differentiate a pathologic vertebral body fracture (associated with an underlying tumor) from an osteoporotic fracture, but involvement of the pedicle or posterior vertebral body suggests metastasis.
A fracture of the lesser trochanter should raise concern for pathologic fracture.
A solitary sternal lesion is highly predictive of metastasis in a patient with breast cancer.
Lytic osseous metastases
Lung (most common purely lytic).
Breast (lytic or blastic).
Thyroid.
Kidney.
Stomach, colon (lytic or blastic).
Blastic (slcerotic) osseous metastases
Breast (lytic or blastic)
Prostate, seminoma.
Transitional cell carcinoma.
Mucinous tumors.
Carcinoid.
Myositis ossificans
Myositis ossificans (MO) is heterotopic bone formation in the skeletal muscle secondary to trauma, although the history of trauma may not be remembered and the trauma may be minor. MO most commonly occurs around the elbow and thigh, which are prone to trauma.
Myositis ossificans may mimic parosteal osteosarcoma. Parosteal osteosarcoma is usually more heavily calcified centrally, while myositis ossificans is typically more calcified peripherally.
If myositis ossificans is suspected, a biopsy should not be performed. A biopsy can lead to unnecessary surgery, as the histology may resemble sarcoma.
The appearance of myositis ossificans eveolves over a period of weeks to months: Weeks 1-2: Soft tissue mass only. Weeks 3-4: Formation of amorphous osteoid matrix. May cause periosteal reaction of adjacent bone. This stage is most suggestive of an early osteosarcoma.
Weeks 5-8: The periphery of the lesion matures into compact bone.
Up to 6 months: Ossification continues to mature.
>6 months: Typically decreases in size.
Brown tumor
A brown tumor is a benign lytic lesion seen in patients with hyperparathryoidism, caused by increased osteoclast activation.
Brown tumor does not have any specific imaging features and may be difficult to differentiate from a giant cell tumor both radiologically and pathologically.
Associated features of hyperparathyroidism are usually present, including: Osteopenia. Subperiosteal bone resorption (especially of the radial aspect of the 2nd and 3rd middle phalanges and the acromial ends of the clavicles). Soft-tissue calcifications.
Lab abnormalities associated with hyperparathyroidism (in addition to elevated PTH level) include elevated calcium and decreased phosphorous.
If hyperparathyroidism is secondary to renal failure, secondary findings of renal osteodystrophy may be seen as well, such as rugger jersey spine.
Osteomyelitis
Osteomyelitis, may cause a permeative or lytic bony lesion that can be indistinguishable from an aggressive malignancy.
Overview of ostomyelitis
Literally meaning “inflammation (-itis) of bone (osteo-) marrow (-myelo-)”, osteomyelitis is infection in bone. Osteomyelitis has protean clinical and imaging manifestations, with an end pathway of chronic progressive bony destruction if untreated.
Osteomyelitis can be classified by route of spread (hematogenous, contiguous spread, or direct inoculation) or by chronicity (acute or chronic), although any route of spread can lead to either acute or chronic disease.
The anatomic distribution and clinical presentation of osteomyelitis are highly dependent on the age of the patient, the specific organism, and the presence of any underlying disorders, wuch as vascular insufficiency or compromised immunity. In adults, osteomyelitis typically arises from either contiguous spread or direct inoculation, such as in diabetic foot infections, open fractures, or as a complication of surgery. Infection is usually polymicrobial. In children, hematogenous spread of infection is mroe common, usually from Staphylococcus aureus.
Terminology of osteomyelitis
Osteitis is inflammation/infection of the cortex.
Periostitis is inflammation/infection of the periosteum.
A sequestrum is a piece of necrotic bone that is separated (sequestered) from viable bone by granulation tissue. A sequestrum is a surgical lesion that can chronically harbor living organisms and function as a nidus for recurrent infection if not resected.
An involucrum is living bone surrouding necrotic bone.
A cloaca is an opening on the involucrum.
A sinus tract is an opening from the infection to the skin surface.
A Brodie abscess is a form of subacute osteomyelitis characterized by central lucency and peripheral sclerosis. The radiographic differential diagnosis of a Brodie abscess is an osteoid osteoma.
Hematogenous osteomyelitis
Acute hematogenous osteomyelitis is usually seen in infants and children. The highly vascularized metaphyses of long bones are most commonly affected. Metaphyseal venules have sluggish flow, which facilitate bacterial invasion.
In infants up to 12 months old, infections can involve the metaphysis, epiphysis, and joint due to the presence of bridging vessels that cross the physis. In older children, infection tends to be isolated to the metaphysis. In adults, the physes are closed but hematogenous metaphyseal infection is uncommon.
Hematogenous infection is typically caused by a single organism. If blood cultures are positive then that specific organism can be targeted and biopsy is generally not needed.
Hematogenous osteomyelitis occurs from teh inside out, beginning with infection of the medullary cavity. Secondary involvement of the cortex occurs as bacteria spread through Haversian and Volkmann canals into the periosteum and subsequently the soft tissues. In infants and children, the periosteum is loosely adherent to the bone, causing prominent lifting of the periosteum by infection. This manifests radiographically as exuberent perostitis. In contrast, in adults the periosteum is more tightly adherent to bone and periostitis is less prominent.
In adults, hematogenous osteomyelitis most commonly affects the spine.
Chronic osteomyelitis may produce infected nonviable tissue (sequestrum). An involucrum is living bone that surrounds the sequestrum. The involucrum may be perforated by cloacae, which can open to the skin to form a sinus tract. Chronic drainage of a sinus tract predisposes to squamous cell carcinoma.
Initial subtle radiographic changes in hematogenous osteomyelitis include focal soft-tissue swelling, regional osteopenia, and obliteration of the soft-tissue fat planes.
The radiographic appearance of medullary infection is a focal, ill-defined lucent metaphyseal lesion. The lucency may cross the epiphysis in young children, where epiphyseal bridging vessels may still be patent. Periosteal reaction may appear aggressive and lamellated, mimicking Ewing sarcoma.
Contiguous focus osteomyelitis
Osteomyelitis is adults is most commonly from contiguous spread of infection, characterized by penetration of the periosteum and cortex and subsequent medullary invasion.
One of the most common causes of adult osteomyelitis is contiguous spread of a diabetic foot ulcer to the bones. Diabetic neuropathy leads to development of foot ulcers due to uncrecognized trauma and impaired vascular reserve.
The primary differential diagnosis of diabetic foot osteomyelitis is a neuropathic joint, a common sequela of diabetic neuropathy. Neuopathic arthropathy usually affects the midfoot and features polyarticular involvement, absence of contiguous soft-tissue infection, and absence of an associated ulcer/sinus tract. The bony cortex is intact. In contrast, diabetic foot osteomyelitis is amost always associated with a cutaneous ulcer and a sinus tract to the bone. The cortex of the involved bone is often disrupted. Abnormal marrow signal is seen in both neuropathic arthropathy and diabetic foot osteomyelitis.
In contrast to hematogenous osteomyelitis, contiguous focus osteomyelitis is typically polymicrobial and biopsy is generally warranted to ensure proper treatment.
Subacute osteomyelitis
Brodie abscess is a characteristic lesion of subacute osteomyelitis, consisting of a walled-off intraosseous infection surrounded by granulation tissue and involucrum.
Chronic osteomyelitis
Chronic osteomyelitis is an indolent infection lasting greater than 6 weeks. Devascularized, necrotic bone leads to a sequestrum surrounded by granulation tissue and involucrum.
Chronic osteomyelitis can cause a mixed lytic and sclerotic appearance, with a thickened cortex.
It can be difficult to differentiate between active and inactive chronic osteomyelitis. Serial radiographs in active chronic osteomyelitis may show development of periosteal reaction.
Sclerosing osteomyelitis, also known as osteomyelitis of Garré, is an uncommon form of chronic osteomyelitis characterized by sclerosis and thickening of bone. The differential diagnosis of sclerosing osteomyelitis includes lymphoma, sclerotic metastasis, and osteoid osteoma.
Specific organisms causing osteomyelitis
Staphylococcus:Staph. aureus is the most common cause of hematogenous osteomyelitis
Salmonella: Osteomyelitis from Salmonella is typically seen in patients with sickle cell disease, with a propensity to affect the diaphysis. It may be difficult to distinguish between diaphyseal bone infarct and osteomyelitis in sickle cell patients.
Pseudomonas: Osteomyelitis from Pseudomonas aeruginosa is classically caused by a puncture wound of the foot through a sneaker.
Tuberculosis: The most common musculoskeletal infection with Mycobacterium tuberculosis is infection of the spine, also known as Pott disease.
Specific locations (osteomyelitis)
Hand and finger: The metacarpals and phalanges may become infected after a bite wound.
Toe: A stubbed great toe with a nail-bed injury is at risk for osteomyelitis of the distal phalanx. due to the location of periosteum immediately adjacent to the nail bed.
Spine: Vertebral osteomyelitis/discitis in an adult may be caused by hematogenous arterial spread, spinal surgery, or spread of a genitourinary infection through the epidural venous Batson plexus. Infection begins in the subendplate region of the vertebral body and subsequently spreads to the endlplate, intervertebral disc, and adjacent vertebral body. In contrast, in children discitis is thought to represent direct hematogenous seeding of the persistently-vascularized disc.
Imaging Osteomyelitis
Radiographs are typically the first modality to evaluate suspected osteomyelitis, although it typically takes between 10-14 days for radiographic changes to be evident.
Radiographic findings depend on the route of spread. Early radiographic changes of hematogenous osteomyelitis include focal osteopenia due to reactive hyperemia, followed by a lucent medullary lesion. In contiguous focus osteomyelitis, the first radiographic sign may be soft tissue swelling and periosteal reaction, followed by erosion of the cortex.
Scintigraphy and MRI imaging are more sensitive to detect early osteomyelitis.
Three-phase Tc-99m MDP bone scan becomes positive within 24-48 hours after the onset of symptoms. Acute osteomyelitis is positive on all three phases (flow, blood pool, and delayed). In contrast, cellulitis is posivite on flow and blood pool phases, and negative on delayed. Although highly sensitive, Tc-99m bone scan is less specific than leukocyte scintigraphy and MRI.
Combining WBC and sulfur colloid scintigraphy adds specificity in the evaluation of osteomyelitis because bone marrow is replaced by infection and white cells. Actively infected bone marrow will show discordantly increased uptake on the WBC scan and reduced activity on sulfur colloid. Note that WBC scan imaging is not sensitive for spinal osteomyelitis, thought to be due to the inability of leukocytes to migrate into an encapsulated infection. WBC scan can be performed with either Indium-111-WBC or Tc-99m-HMPAO-WBC. Indium WBC scan has higher radiation dose, takes 24 hours to perform, and the image has more noise. The disadvantage of Tc-99m-HMPAO is its tendency to dissociate, leading to genitourinary excretion of radiotracer.
MRI is highly sensitive to detect early osteomyelitis within 3-5 days. MRI has similar sensitivity to radionuclide studies, but greater specificity. MRI can better delineate the extent of infection, any fluid collections that must be treated surgically, sinus tracts, and skin ulcers.
The hallmark of MRI imaging of osteomyelitis is replacement of the normal fatty marrow signal. Edema and exudates cause high marrow signal on T2-weighted images and low signal on T1-weighted images. Increased signal of the cortical bone, normally low signal on all sequences, signifies infectious involvement MRI has very high negative predictive value: A negative MRI essentially excludes osteomyelitis. Gadolinium is helpful to delineate any fluid collections and to evaluate for the presence of nonenhancing necrotic bone (sequestrum).
Septic arthritis
Septic arthritis is infection of a joint. The gold standard for diagnosis of septic arthritis is joint aspiration.
The imaging and clinical hallmark of septic arthritis is a joint effusion.
In children, the hip is a common site of septic arthritis caused by contiguous extension of proximal femoral metaphyseal osteomyelitis. The proximal femoral metaphysis is within the hip joint capsule.
If untreated, septic arthritis can lead to rapid joint destruction and eventual ankylosis.
Intravenous drug abusers are susceptible to infection of the sacroiliac and acromioclavicular joints.
Necrotizing fasciitis
Necrotizing fascitis is an extremely aggressive soft tissue infection caused by Clostridium or other gram-positive rods. It is a surgical emergency, requiring immediate debridement.
The characteristic radiographic and CT finding of necrotizing fasciitis is gas bubbles in the soft tissues.
Osteoporosis
Osteoporosis is the most common metabolic bone disease and is defined as a T score of < -2.5, where a T score of -1 is a bone density one standard deviation below the mean for healthy young women. The Z score is the standard deviations from age-matched women. It is not used to determine osteoporosis.
Osteopenia may be secondary to numerous nutritional, endocrine, and other etiologies.
Vitamin or nutritional deficiencies can cause osteoporosis, including: Osteomalacia (looser zone). Alcoholism, Hypophophatemia, Scurvy (Wimberger sign).
Endocrine disturbances can impact calcium metabolism, causing osteoporosis, including: Hyperparathyroidism (subperiosteal resorption), Cushing disease or any increase in endogenous/exogenous steroids.
Diffuse malignancy, such as myelomatosis, can cause diffuse bony demineralization.
Genetic causes of osteoporosis include: Osteogenesis imperfecta, Gaucher disease, Anemia including sickle cell and thalassemia.
Focal osteopenia has a more limited list of causes, including: Immobility/disuse, reflex sympathetic dystrophy, transient regional osteoporosis of the hip.
Scurvy
Scurvy (hypovitaminosis C) causes generalized osteopenia because osteoblasts require vitamin C to form mature osteoid tissue.
Other signs of scurvy include the Wimberger ring sign, which is increased epiphyseal sclerosis due to disorganized epiphyseal ossification, and a Pelkin’s fracture, which is a metaphyseal corner fracture. A dense metphyseal line may be present.
Osteomalacia
Osteomalacia is faulty mineralization of bone matrix caused by vitamin D deficiency. The same process is called osteomalacia in adults and rickets in children. Rickets is discussed in the pediatric imaging section.
Osteomalacia manifests as diffuse osteopenia; however, a Looser zone (pseudofracture) is highly specific. A Looser zone is a cortical stress fracture that is filled with abnormal, poorly mineralized osteoid and appears as a radiolucency through the cortex. Common sites for Looser zones are the medial proximal femurs, distal scapulae, and pubic bones.
Osteomalacia may be complicated by insufficiency fracture.
Acromegaly
Acromegaly is the clinical syndrome caused by excess growth hormone. When the growth hormone excess occurs when the physes are open, the bones will grow longitudinally, leading to gigantism. However, when the hormone excess occurs once the physes have closed then the bones cannot lengthen and intead obtain a characteristic appearance of acral (disal) growth and widening.
In the head there is enlargement of frontal sinuses, thickening of cranial bones, and an enlarged jaw.
In the hands, beak-like osteophytes of the metacarpal heads and spade-like overgrowths of the distal phalanges are characteristic. Initially, joint spaces are widened, but may become narrowed later in the disease due to secondary osteoarthritis.
In the feet, a characteristic finding is increased heel-pad thickness greater than 24 mm. 24 mm is normal heel-pad thickness for a 150lb person, with approximately 1 mm allowed for each additional 25 lb in body weight. For instance, a 250 lb perosn may have a heel-pad of 28 mm.
Hyperparathyroidism (Recklinghausen disease of bone)
Hyperparathyroidism is excess parathyroid hormone (PTH). PTH is normally secreted in response to hypocalcemia and maintains serum calcium levels by stimulating osteoclasts.
Primary hyperparathyroidism is autonomously increased secretion from an overactive parathyroid gland, typically due to a parathryoid adenoma. Serum calcium is high and phosphate is low.
Secondary hyperparathyroidism is increased secretion of PTH by a normal gland in response to hypocalcemia secondary to renal failure. Serum calcium is usually normal.
Tertiary hyperparathryoidism is seen after prolonged secondary hyperparathyroidism, where the parathyroid glands escape regulatory control and oversecrete PTH.
The radiological hallmarks of hyperparathyroidism are diffuse bony demineralization and subperiosteal and subligamentous bone resorption.
Skull: The classic salt-and-pepper skull is due to trabecular resorption.
Hands: Subperiosteal resorption of the radial aspects of the 2nd and 3rd middle phalanges is specific for hyperparathyroidism.
Clavicle: Subperiosteal resorption of the clavicle tends to affect the acromial (distal aspect).
Knee: Subperiosteal obne resorption can be seen in the medial proximal tibial metaphysis.
Teeth: Loss of lamina dura surrounding the tooth socket can occasionaly be seen.
Anywhere: Brown tumors are more common in primary hyperparathyroidism.
Everywhere: Diffuse osteopenia results from continued osteoclast activation.
Calcium pyrophosphate dihydrate deposition (CPPD) may occur, which is more common in primary hyperparathyroidism.
Soft-tissue calcification, periosteal reaction, and sclerosis are seen more commonly in secondary hyperparathyroidism.
Complications of hyperparathyroidism include insufficiency fracture and increased propensity for ligaments and tendons to rupture.
Differntial diagnosis of common bone lesions
Basics of Trauma
When describing a long-bone fracture, the fracture locations (proximal, mid-shaft, distal), direction of the fracture, angulation, and position of the distal segment should be described.
A comminuted fracture is defined as >2 fracture fragments.
It is essential to mention if a fracture extends to the articular surface of a joint.
A stress fracture may be a fatigue fracture (abnormal repetitive stress on a normal bone) or an insufficiency fracture (normal stress on an abnormal bone; e.g. in the setting of demineralization due to osteoporosis or metabolic bone disease). The term stress fracture is often used interchangeably with fatigue fracture, although these terms are not synonyms.
A pathologic fracture is caused by normal stress on a bone weakened by an underlying lesion (typically tumor, but also including infection, fibrous dysplasia, and Paget disease).
Forefoot
Lisfranc fracture-dislocation
The tarsometarsal joint is the Lisfranc joint, named after the French surgeon in the Napoleonic wars who performed amputations at this joint. The stability of the joint depends on multiple ligaments, with the Lisfranc ligament being the most important. The Lisfranc ligament is an interosseous ligamentous complex attaching the medial cuneiform to the second metatarsal base.
A Lisfranc fracture-dislocation is a fracture-dislocation of the tarsometatarsal joint. The treatment of a Lisfranc injury is surgical. A missed or untreated Lisfranc injury can lead to debilitating osteoarthritis and flattening of the longitudinal arch.
Subtle malalignment of teh tarsometatarsal joint may signal serious ligamentous injury. Weight-bearing radiographs are the most sensitive. Careful evaluation of the alignment of the Lisfranc joint must always be performed, as in this normal example below.
Lisfranc injuries are classified into homolateral and divergent based on the direction of dislocation of the first metatarsal. In a divergent Lisfranc injury, the first metatarsal is medially dislocated and the 2nd through 5th metatarsals are laterally dislocated. In homolateral injury, all metatarsals will dislocated laterally.
Midfoot and Hindfoot
Ankle Tendon Anatomy
Medial Ankle ligament anatomy
Arranged from medial to lateral, the anterior extensor tendons can be remembers witht he mnemonic Tom, Harry, and Dick (Tibialis anterior, Extensor Hallucis longus, Extensor Digitorum longus)
The anterior tibial artery runs anteriorly with the extensor tendons.
Normal menisci anatomy
The medial and lateral menisci are crescent-shaped fibrocartilaginous structures that form a discontinuous figure-eight to stabilize the knee and disperse the axial loading.
Each meniscus consists of an anterior and a posterior horn. The posterior horn of the medial meniscus is larger than its anterior horn. Both horns of the lateral meniscus are the same size.
Each meniscus is attached to the tibial plateau by an anterior and posterior meniscal root. Trauma to the meniscal root may cause meniscal extrusion.
There are two meniscofemoral ligaments, which extend from the posterior horn of the lateral meniscus to the medial femoral condyle. It is important not to mistake a meniscofemoral ligament (which are variably present) for a meniscal tear. The ligament of Humphry is anterior to the PCL; the ligament of Wrisberg is posterior to the PCL.
The peripheral third of each meniscus is relatively vascular and is called the red zone. The central portion of the meniscus is considered avascular.
Meniscal injuries confined to the red zone may heal spontaneously or after surgical repair, while more central meniscal injuries generally do not heal.
Oblique/horizontal meniscal tears
The terms oblique and horizontal are sometimes used interchangeably when referring to meniscal tears. Strictly speaking, however, a horizontal tear remains parallel to the tibial plateau, while an oblique tear may be at a slight angle to the tibial plateau.
An oblique/horizontal tear is the most common meniscal tear, typically occurring in the posterior horn of the medial meniscus.
Oblique and horizontal tears are more often degenerative, rather than due to trauma.
Vertical/longitudinal tear
The vertical (synonymous with longitudinal) tear is a curved tear that follows the contour of the meniscus. On serial sagittal images, the tear will be in a vertical orientation and will remain a fixed distance fromt he edge of the meniscus.
Bucket-handle meniscal tear
A bucket handle tear is the result of an extensive vertical tear, occurring when the free inner edge of the meniscus (medial meniscus most commonly) gets displaced or flipped over.
The most sensitive imaging finding of a bucket-handle tear is teh absent bow tie sign, seen when there are fewer than two “bow ties” on adjacent 4 mm-thick sagittal slices.
The most common location of the displaced meniscal fragment is the intercondylar notch, but the meniscal fragment may also displace anteriorly or posteriorly.
Anterior displacement produces the double delta sign on sagittal MRI (either meniscus).
Posterior displacement produces the double PCL sign on sagittal MRI (medial meniscus only).
Radial/transverse meniscal tear
A radial tear (also known as a transverse tear) is a vertically oriented tear that is perpendicular to the arc of the meniscus. In contrast, the previously discussed vertical/longitudinal tear follows the curve of the meniscus.
On a single image, a radial tear may be indistinguishable from a vertical/longitudinal tear. On serial sagittal images, however, the radial tear will change position relative to the edge of the meniscus. This phenomenon is the marching cleft sign.
Depending on the orientation of the tear in relation to the scan plane, a radial tear may also show the ghost meniscus sign. The ghost meniscus is typically described as absence of the posterior horn of the meniscus on sagittal images (although is may also occur with absence of the anterior horn, as seen above). It occurs in tears adjacent to the intercondylar notch.
Radial tears are associated with a high rate of meniscal extrusion, which may lead to osteoarthritis if not treated.
Discoid Meniscus
Discoid meniscus is a spectrum of congenital malformations of the meniscus that ranges from increased thickness of the meniscus to a complete disc-like shape. Discoid meniscus is defined by having a portion of the meniscus extending to the central tibial plateau.
Discoid meniscus typically affect children and is a common cause of joint-line pain, clicking, or locking in a child or adolescent. Discoid meniscus is prone to undergo cystic degeneration and tear. Even in the absence of a tear, a discoid meniscus may be symptomatic.
The lateral meniscus is more commonly affected.
On MRI, a meniscus is discoid if an oval or bow tie-shaped meniscus is seen on three or more contiguous sagittal slices with standard 4 mm-thick sagittal slices (representing 12 mm medial-lateral thickness).
Hip Anatomy
The acetabulum is formed by the fusion of three bones: The ilium superiorly, the pubis anterioly, and ischium posteriorly.
Pediatric radiographs of the hip clearly show the separation of these three bones, which meet at the triradiate cartilage to form the acetabulum.
The articular surface of the acetabulum is lined by a horseshoe-shaped thin articular cartilage. The center of the acetabulum, called the pulvinar, is not covered by cartilage.
The labrum forms a fibrocartilaginous ring approximately 270 degrees around the periphery of the acetabulum. The labrum blends with the transverse ligament anterior/inferiorly. Note that there is no labrum at the anterior/inferior aspect of the acetabulum where the transverse ligament lies.
The transverse ligament gives off fibers that form the ligamentum teres, which connects to the femoral head at its central fovea.
The femoral head is mostly covered by articular cartilage except at the fovea capitis (central fovea), which is a central depression and attachment site to the ligamentum teres.
The greater and lesser trochanters are apophyses. The greater trochanter is the insertion site for the gluteus medius, gluteus minimus, obturator internus and externus, and the piriformis. The lesser trochanter is the insertion site for the iliopsoas. A lesser trochanteric fracture in an adult is considered pathologic until proven otherwise.
Femoral neck fracture (intracapsular)
Femoral neck fractures can be divided into three categories based on location: Subcapital (directly below the femoral head), transcervical (through the neck), and basicervical (at the base of the femoral neck). Subcapital fractures are the most common.
The Garden classification of subcapital femoral neck fractures is based on the degree of valgus displacement and is commonly used by radiologists. Note that varus is defined as an angle with apex pointed laterally and valgus is defined as an angle with apex pointed medially (mnemonic: “fair” Lady and “vulgar” Mouth)
Stage I: Impacted or incomplete femoral neck fracture, with valgus orientation of the femoral head/neck trabeculae and varus orientation of the femoral head and acetabulum. The femoral shaft is externally rotated. The medial trabeculae of the femoral head and neck form an angle >180º. This fracture is stable and has a good prognosis.
Stage II: Complete, nondisplaced fracture. The trabeculae of the femoral head and neck are in mild varus and form an angle of approximately 160º. This fracture also has a good prognosis.
Stage III: Complete, partially displaced fracture. There is more marked varus alignment of the trabecular pattern of the femoral head and neck, usually forming an angle <160º.
Stage IV: Complete, displaced fracture. The trabecular pattern of the femoral head is aligned with that of the acetabulum, which is the normal anatomic alignment.
The Boyd-Griffin and Evans classification are used to describe intertrochanteric fractures by orthopedists. These classifications are rarely used by radiologists.
Fractures at or inferior to the lesser trochanter are subtrochanteric fractures. Subtrochanteric fractures are classified using the Fielding or Seinsheimer classifications by orthopedists.
Garden classification of subcaptial femoral neck fractures
Cervical spine trauma
Intervals: The basion-dental interval and atlanto-dental interval (also known as the atlanto-axial interval) should be evaluated in every lateral cervical spine radiograph. An increased basion-dental interval >12 mm suggests craniocervical dissociation. An increased atlanto-dental interval >2.5 mm (some authors suggest 3 mm as a cutoff) can be seen in ligamentous laxity and resultant subluxation.
Lines: Every lateral cervical spine radiograph should be evaluated for continuity and smoothness of the four primary osseous contours.
Anterior vertebral line: Traces the anterior margin of the vertebral bodies. The prevertebral soft tissues are located anterior to the anterior vertebral line.
Posterior vertebral line: Traces the posterior margin of the vertebral bodies and the anterior margin of the spinal canal. The spinal canal is the space between the posterior vertebral and spinolaminar lines.
Spinolaminar line: Traces the posterior margin of the spinal canal.
Spinous process line: Traces the posterior tips of the spinous processes.
Overview of named cervical spine fractures
Bony anatomy of the shoulder
Dislocations and associated sequela
Acromial shape and orientation
The impact of acromialshape on impingement syndrome is controversial. An acromion with a hooked undersurface (type III) or convex undersurface (type IV) may contribute to impingement (primary external type) and lead to subsequent rotator cuff tears.
Friction of the acromion against the immediately underlying supraspinatus and biceps tendons may predispose to injury from impingement.
Rotator cuff anatomy
The rotator cuff is an essential active stabilizer of the glenohumeral joint and is formed by the four rotator cuff muscles (supraspinatus, infraspinatus, teres minor, and subscapularis) and their tendons.
The supraspinatus, infraspinatus, and teres minor are located posterior to the body of the scapula and insert on the greater tuberosity. The subscapularis is anterior to the scapula and insert on the greater tuberosity. The subscapularis is anterior to the scapula and inserts on the lesser tuberosity.
Anatomy of the shoulder ligaments
The rotator interval is a triangular region that allows rotational motion around the coracoid process. It is located between the supraspinatus and subscapularis tendons. The rotator interval contains the coracohumeral ligament (CHL), the long head of the biceps tendon (LHBT), and the superior glenohumeral ligament (SGHL).
The CHL connects the lateral aspect of the coracoid process to the greater tubercle of the humerus, where the CHL blends with the supraspinatus tendon. The CHL helps to stabilize the intraarticular biceps tendon together with the superior glenohumeral ligament as the biceps pulley. The CHL is located external to the joint capsule.
The three glenohumeral ligament (SGHL) connects the lesser tuberosity to the supraglenoid tubercle of the scapula.
The middle glenohumeral ligament (MGHL) also connects the lesser tuberosity to the supraglenoid tubercle of the scapula. The MGHL is congenitally absent in up to one third of patients. Tears of the MGHL are associated with superior labral tears.
The inferior glenohumeral ligament (IGHL) connects the anatomic neck of the humerus to the inferior glenoid labrum. The IGHL is by far the most important component of the capsulolabral complex for maintaining stability in abduction and external rotation. The IGHL contains three components (the anterior band, the axillary pouch, and the posterior band), all of which are well-seen on sagittal MR: The anterior band of the IGHL provides anterior stability. There are several lesions of the anterior band of the IGHL that are associated with anterior instability. The IGHL forms the axillary pouch of the glenohumeral joint capsule. The posterior band contributes to posterior stability. The IGHL is the only glenohumeral ligament to have a posterior component.
The long head of the biceps tendon (LHBT) attaches to the anterosuperior glenoid rim along with the SGHL and MGHL.
Suprascapular nerve entrapment at the spinoglenoid notch
The distal suprascapular nerve provides motor innervation to the infraspinatus muscle only. Entrapment of the distal suprascapular nerve at the spinoglenoid notch will cause isolated atrophy of the infraspinatus.
Common Hand and Wrist fractures
Lunate aned perilunate dislocation
In a perilunate dislocation, the lunate is aligned with the radius, but capitate is not aligned with the lunate. Dislocation is next to the lunate (peri-lunate).
In a lunate dislocation, the lunate is dislocated volarly, but the capitate is still relatively aligned with the radius. The lunate itself is dislocated (lunate dislocation).
Extension tendon injuries
Mallet finger: Mallet finger is disruption of the extensor tendon at the distal phalanx. It is caused by direct impact on the tip of the finger. Mallet finger may be associated with an avulsion fragment of the distal phalanx, which is clinically an important distinction.
On physical exam, the distal interphalangeal (DIP) joint cannot be straightened.
Boutonniere deformity is injury to the medial slip of the extensor tendon. It is seen most commonly in the setting of rheumatoid arthritis, but it may be post-traumatic.
The proximal interphalangeal (PIP) joint herniates through the lateral slips of the common extensor tendon and becomes entrapped, causing fixed flexion of the PIP and extension of the DIP.
